The Revolution of Hepatitis C Treatments:

Review for Nurse Practitioners

Mary C. Olson, DNP, ANP-BC, Donald Gardenier, DNP, FNP-BC, and
Ira M. Jacobson, MD
ABSTRACT

Chronic hepatitis C virus infection has a widespread presence in the worlds

population. Because of its potential for liver decompensation and secondary
manifestations, hepatitis C virus has been the subject of many clinical trials over the
past 20 years. This article will delineate the results of these various studies. The
interferon-free regimens with combinations of all oral antiviral combinations will
provide improved tolerability and efcacy with sustained viral response rates greater
than 90%. The outcomes and the commonly accepted methodologies for treatment,
according to patient requirements, will be provided for the primary care nurse
practitioner.
Keywords: cirrhosis, direct-acting antiviral, hepatitis C, interferon free, liver disease,
nurse practitioner, treatment experienced, treatment naive
2015 Elsevier, Inc. All rights reserved.

he hepatitis C virus (HCV) is a global

scourge. Anywhere from 130 million to 180
million people around the world are infected
with the virus.1 Because of its widespread presence in
the worlds population, HCV has been the subject of
many clinical trials over the past 20 years. This article
delineates the results of these various studies, showing
the efcacy and safety of new interferon-free regimens. These results will revolutionize the treatment
of hepatitis C. The outcomes and the commonly
accepted methodologies for treatment, according to
patient requirements, are provided. The purpose of
this article is to discuss the treatment of patients
diagnosed with HCV for the primary care nurse
practitioner (NP).
EVOLUTION OF HCV TREATMENT

HCV is a RNA virus that infects hepatocytes. There

are 6 HCV genotypes with different structures
requiring specic treatment approaches. Initially, the
standard of care for HCV was interferon alpha
monotherapy with response rates from 15%-20%.2 In
1998, combination therapy with interferon alpha and
ribavirin for 24-48 weeks, depending on the HCV
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genotype, was approved. The overall sustained viral

response (SVR) rates 24 weeks after stopping therapy
(SVR24) for this regimen were 31%-38%.3 In 2000
and 2001, pegylated interferons in combination with
ribavirin were approved with SVR24 response rates
of 40%-56%.4,5
Direct-acting antiviral (DAA) medications have
been developed that target proteins encoded by the
viral genome. The targets are the NS3/4A protease,
NS5A, and the RNA polymerase. In 2011, the rst
DAA medications for HCV genotype 1 were
approved. These were the protease inhibitors boceprevir in combination with pegylated interferon and
ribavirin or telaprevir in combination with pegylated
interferon and ribavirin. The SVR24 rates for these
regimens were 68%-75%, respectively.6,7 The side
effect prole was increased with the addition of these
protease inhibitors to the pegylated interferon and
ribavirin regimen. Thus, regimens needed to be
developed that would have improved efcacy and
tolerability.
In 2013, a protease inhibitor, simeprevir, and a
nucleotide polymerase inhibitor, sofosbuvir, were
approved (each to be prescribed in combination with
Volume 11, Issue 1, January 2015

pegylated interferon and ribavirin for genotype 1

patients). Sofosbuvir with pegylated interferon and
ribavirin was also approved for genotype 4 patients.8
The response rate for sofosbuvir with pegylated
interferon and ribavirin is 89% for HCV genotype 1
patients naive to prior therapy.9 Sofosbuvir with
ribavirin was approved for the treatment of patients
with HCV genotypes 2 and 3.8
CURRENT HCV TREATMENT

The current standard of care for HCV genotype 1

patients who are treatment naive or have failed prior
therapy is the xed-dose combination tablet of
ledipasvir 90 mg and sofosbuvir 400 mg called
Harvoni (Gilead Sciences, Foster City, CA). The
treatment is 1 tablet orally daily for 12 weeks for
HCV genotype 1 patients who are treatment naive or
treatment experienced without cirrhosis. HCV genotype 1 patients who are treatment experienced
with cirrhosis will be treated for 24 weeks. Eight
weeks treatment duration can be considered for
HCV genotype 1 patients who are treatment naive
without cirrhosis and have a pretreatment HCV viral
load < 6 million IU/mL. The most common side
effects are fatigue and headache.10
HCV genotype 1 patients are treated with sofosbuvir and weight-based ribavirin for 24 weeks. The
response rate for this regimen for treatment-naive
patients, most of whom were noncirrhotic, was 68%
or 17 of 25 patients.11 Patients with advanced brosis
were more likely to relapse.11
HCV genotype 2 treatment-naive and prior
treatment failure patients can recommended to be
treated for 12 weeks with sofosbuvir 400 mg orally
daily and weight-based ribavirin 1,000 mg (< 75 kg)
or 1,200 mg (
75 kg) in divided doses orally daily
with overall SVR rates of 78% (161/207) for patients
who were ineligible for interferon and 93% (68/73
patients) for treatment-naive and prior treatment
failure patients.8,12,13 The recommended treatment
for HCV genotype 3 patients is sofosbuvir 400 mg
orally daily and weight-based ribavirin 1,000 mg (<
75 kg) or 1,200 mg (
75 kg) in divided doses daily
for 24 weeks with an overall SVR rate 12 weeks after
stopping therapy (SVR12) of 85% (213/250 patients).
This is lower (60%) in treatment-experienced patients
with cirrhosis.8,13
www.npjournal.org

HCV genotype 4 treatment-naive patients who

are eligible for interferon are recommended to be
treated with sofosbuvir 400 mg and weight-based
ribavirin 1,000 mg (< 75 kg) or 1,200 mg (
75 kg)
and pegylated interferon for 12 weeks. The overall
response rate is 96% (27/28 patients).8,9
Interferon-ineligible patients with HCV genotype
4 are recommended by the American Association for
the Study of Liver Disease and Infectious Disease
Society of America (IDSA) to be treated with
sofosbuvir 400 mg orally daily plus weight-based
ribavirin 1,000 mg (< 75 kg) or 1,200 mg (
75 kg)
orally for 24 weeks.8 Eleven of 14 treatment-naive
genotype 4 patients treated with this regimen achieved SVR12 for a response rate of 79%.8
Interferon is an immune modulator that increases
the immune response against HCV. Interferon has
been associated with considerable side effects. The
side effects include u-like symptoms, fatigue,
nausea, loss of appetite, psychiatric symptoms, hair
loss, neutropenia, and thrombocytopenia. Rarely,
interferon can cause retinopathy, ototoxicity, neuropathy, hypothyroidism, and diabetes.2 Interferon is
contraindicated in patients with certain comorbid
medical conditions including autoimmune and
psychiatric disorders. Interferon-free regimens have
been needed for the treatment of HCV in order to
treat patients who are ineligible for interferon and
to improve the safety and tolerability of HCV
treatment.
Combinations of two or three DAAs have been
developed to improve the tolerability and efcacy of
HCV treatment regimens. DAAs have been developed that target proteins on the viral genome, the
NS3/4A protease, NS5A, and the polymerase.
Inhibiting these proteins during viral replication
prevents the virus from being able to reproduce and
causes eradication of the virus from hepatocytes.14
DAAs Approved and Pending Food and Drug
Administration Approval

DAA combinations include all oral combinations of

two or three DAAs from different classes (Table 1).
The combinations evaluated in large trials thus far
include a protease inhibitor with a NS5A inhibitor; a
protease inhibitor with a polymerase inhibitor; a
NS5A inhibitor with a polymerase inhibitor; and a
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117

Table 1. HCV Direct Acting Antiviral Medications

Drug Name

Protease
Inhibitor

Boceprevira

NS5A
Inhibitor

Telaprevir

Simeprevir

Asunaprevir

ABT450

X
a

Polymerase
Inhibitor

Sofosbuvir

X (nucleotide)

Dasabuvir

X (nonnucleotide)
a

Ledipasvir

Daclatasvir

Ombitasvir

Approved direct-acting antivirals.

protease inhibitor, NS5A inhibitor, and a

nonnucleotide polymerase inhibitor with or without
ribavirin.14
The following are anticipated DAA combinations
that are expected in late 2014. These regimens are
those for which lings have been made to the Food
and Drug Administration for approval (Table 2).14
The all-oral combinations of two or three DAAs
with or without ribavirin will increase the tolerability
and efcacy of HCV regimens. These combinations
will be able to decrease the duration of treatment to
8, 12, or 24 weeks depending on the patient
population.14
The combination of a nucleotide polymerase inhibitor, sofosbuvir, and a NS5A inhibitor, ledipasvir,
has been tested in clinical trials that included
treatment-naive and treatment-experienced patients
with chronic HCV infection. These trials included
patients with cirrhosis and patients who had prior
exposure to protease inhibitors. The ION-1 trial, a

phase 3, open-label study, included previously untreated patients with chronic HCV genotype 1a and
1b infection who were treated with sofosbuvir 400
mg and ledipasvir 90 mg xed-dose tablets once daily
by mouth for 12 weeks or 24 weeks with and
without ribavirin. Sixteen percent of the study population had cirrhosis, and 12% were black. Among
214 patients who received sofosbuvir, ledipasvir, and
ribavirin for 12 weeks, 211 achieved SVR12 (99%).
Among the 217 patients who received sofosbuvir and
ledipasvir without ribavirin, 211 achieved SVR12
(97%). The duration of 24 weeks and the addition of
ribavirin did not improve response rates to this
regimen.15 The most common adverse events
reported were fatigue, headache, insomnia, and
nausea. These adverse events were in the mild to
moderate range.15
The ION-2 trial, a phase 3, randomized, openlabel study, included patients with chronic HCV
genotype 1a and 1b who were previously treated
with pegylated interferon and ribavirin. Fifty-two
percent of patients had been treated previously with a
protease inhibitor containing regimen; 20% of the
patients had cirrhosis. Patients were given sofosbuvir
400 mg and ledipasvir 90 mg xed-dose tablets once
daily by mouth for 12 weeks or 24 weeks with and
without ribavirin. The SVR12 rate for patients who
received 12 weeks of treatment without ribavirin was
94% (102/109), and with ribavirin it was 96% (107/
111). The SVR12 rate for patients who received 24
weeks with ribavirin (110/111 patients) and without
ribavirin (108/109 patients) was 99%.17 The most
common adverse events were fatigue, headache, and
nausea. These adverse events were in the mild to
moderate range.16
The LONESTAR study compared sofosbuvir 400
mg and ledipasvir 90 mg xed-dose tablets once daily

Table 2. HCV Direct Acting Antiviral Regimens

Protease Inhibitor

NS5A Inhibitor

NA

Ledipasvir

Sofosbuvir (nucleotide)

Polymerase Inhibitor

Guanosine (Ribonucleic) Analog

ABT450/ritonavir

Ombitasvir

Dasabuvir (nonnucleotide)

With or without ribavirin

Simeprevir

NA

Sofosbuvir

With or without ribavirin

Daclatasvir

Sofosbuvir

NA not applicable.

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Volume 11, Issue 1, January 2015

with and without weight-based ribavirin (< 75 kg

1,000 mg and
75 kg 1,200 mg) for 8 weeks versus
12 weeks of sofosbuvir and ledipasvir xed-dose
tablets without ribavirin in treatment-naive patients
with HCV genotype 1 infection. The SVR12 rate for
treatment-naive noncirrhotic patients treated for 8
weeks with sofosbuvir and ledipasvir without ribavirin was 95% (19/20 patients), and with ribavirin it
was 100% (21/21 patients). The SVR12 rate for 19
treatment-naive noncirrhotic patients treated for 12
weeks with sofosbuvir and ledipasvir was 100% (one
patient was lost to follow-up but had achieved SVR
8 weeks after stopping treatment). Patients previously
treated with a regimen containing a protease inhibitor were treated for 12 weeks with sofosbuvir and
ledipasvir with and without ribavirin. Eighteen of 19
patients (95%) achieved SVR12 after 12 weeks of
treatment with sofosbuvir and ledipasvir without
ribavirin. All 21 patients (100%) treated for 12 weeks
with sofosbuvir and ledipasvir with ribavirin achieved SVR12.17
The regimen of ABT450/r, ombitasvir, and
dasabuvir with ribavirin for 12 weeks was studied in
patients with HCV genotype 1 infection without
cirrhosis who were previously treated with pegylated
interferon and ribavirin and failed to achieve SVR
(SAPPHIRE-II). Of the 297 patients treated, 286
patients (96%) achieved SVR12. The most common
adverse events were headache and fatigue. These
adverse events occurred in 36.4% and 33.3% of the
patients, respectively, and were mild.18
Patients with HCV genotype 1 infection with
cirrhosis who were naive to treatment or treatment
experienced were also included in a clinical trial
(TURQUOISE II) with ABT450/r, ombitasvir,
dasabuvir, and weight-based ribavirin. Patients were
randomly assigned to 12 or 24 weeks of treatment.
Among 208 patients treated for 12 weeks, 191
(91.8%) achieved SVR12. There were 172 patients
treated for 24 weeks, and 165 (95.9%) achieved
SVR12. The difference was driven largely by genotype 1a prior null responders, leading to the
conclusion that such cirrhotic patients are best treated
for 24 weeks with this regimen. The most common
adverse events were fatigue, headache, and nausea.19
Clinical trials that included the interferon-free
regimen of ABT450 with ritonavir (ABT450/r),
www.npjournal.org

ombitasvir (at once daily dosing of 150 mg ABT450,

100 mg ritonavir, and 25 mg ombitasvir), and dasabuvir (250 mg 2 times daily) with or without ribavirin (1,000 mg or 1,200 mg daily) were conducted
in patients who were infected with HCV genotype 1
without cirrhosis and were naive to treatment. One
phase 3 study (PEARL-III) included patients infected
with HCV genotype 1b, and another phase 3 study
(PEARL-IV) included patients infected with HCV
genotype 1a. Patients in both studies were given the
interferon-free regimen of ABT450/r, ombitasvir,
and dasabuvir with or without ribavirin for 12 weeks.
Among 210 patients with HCV genotype 1b infection treated for 12 weeks with ABT450/r, ombitasvir, and dasabuvir with ribavirin, 209 (99.5%)
achieved SVR12. The regimen of ABT450/r,
ombitasvir, and dasabuvir without ribavirin given for
12 weeks to 209 patients resulted in 207 (99.0%) who
achieved SVR12. HCV genotype 1a patients were
treated for 12 weeks with ABT450/r, ombitasvir, and
dasabuvir with ribavirin that resulted in 97 of 100
(97.0%) patients with SVR12. Of the 205 patients
who received the regimen without ribavirin, 185
(90.2%) achieved SVR12.19 Thus, ribavirin appears
to improve SVR rates with this regimen for patients
infected with HCV genotype 1a who have never
been treated before. The most common adverse
events for this regimen were headache and fatigue. In
the ribavirin-containing groups, other common
adverse events were pruritus, nausea, and insomnia
and were mild.20
Daclatasvir, a NS5A inhibitor, was studied in
combination with asunaprevir, a protease inhibitor
for HCV genotype 1b infection. SVR24 rates were
80.5% to 90.9%.21 Daclatasvir and sofosbuvir were
studied together in treatment-naive and treatmentexperienced patients with chronic HCV genotype 1,
2, or 3 infection. Daclatasvir 60 mg daily with
sofosbuvir 400 mg daily with or without ribavirin was
given for 12 or 24 weeks to treatment-naive patients
with HCV genotype 1, 2, or 3. An additional study
group was added that included patients who had
failed a treatment regimen containing the protease
inhibitor boceprevir or telaprevir. These patients
were treated for 24 weeks with daclatasvir 60 mg and
sofosbuvir 400 mg daily with or without ribavirin.
The overall SVR12 rate was 98% (164/167) for
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119

patients with HCV genotype 1 infection including

treatment-naive or prior protease inhibitor treatment
failures. Ninety-two percent (24/26) of patients with
HCV genotype 2 infection and 89% (16 of 18) of
patients with HCV genotype 3 infection achieved
SVR12. The most common adverse events were
fatigue, headache, and nausea.22
Simeprevir, a protease inhibitor, and sofosbuvir
with or without ribavirin have been prescribed
together as an off-label interferon-free regimen to
treat HCV genotype 1 patients. Both drugs were
approved in 2013, recognizing that the oral combination is itself off-label. Data from the phase 2
COSMOS trial support the use of this regimen. The
study provides data from 2 cohorts. Cohort 1
included patients with HCV genotype 1 infection
with mild to moderate brosis (METAVIR scores
F0-F2). These patients were treated with simeprevir
150 mg daily in combination with sofosbuvir 400 mg
daily with or without weight-based ribavirin for
12 weeks. The SVR12 rates were 96% (26/27 patients) and 93% (13/14 patients), respectively.
Cohort 2 included patients with HCV genotype 1
infection with advanced brosis (METAVIR scores
F3-F4). SVR12 rates were 94% (82/87 patients) for
both the ribavirin-containing group and the no
ribavirin group.23,24 (Initial evaluation of the HCV
patient is covered by the article in this issue by
Gardiner et al.)
CONSIDERATIONS FOR TREATMENT

The selection of a treatment regimen will be determined by several factors. These include HCV genotype, treatment history, stage of brosis,
medications for comorbid medical conditions, and
adherence factors.
The HCV genotype will determine the treatment
options available. Resistance testing with the Genosure (LabCorp, Uniondale, NY) test can be considered to assist in determining the best treatment
regimen. For example, Q80K sequence variation
occurs in 40% of patients with HCV genotype 1a and
decreases the effectiveness of the protease inhibitor
simeprevir in patients who are less sensitive to PEG/
RBV.25 It is not clear if the Q80K variation decreases
the effectiveness of simeprevir when combined with
sofosbuvir. Also, resistance testing determines if the
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patient has resistance to protease inhibitors when they

have previously failed a regimen that contained a
protease inhibitor. If resistance to a protease inhibitor
exists, a regimen that does not contain a protease
inhibitor would be selected for the patient.
Stage of brosis and treatment history will
determine treatment duration. Data indicate that
treatment-experienced patients with cirrhosis have
better SVR rates if treated for 24 weeks than
12 weeks.10,14
Drug-drug interactions (DDIs) are another
consideration when treating patients with the DAA
combination HCV treatments. Based on the mechanism by which a medication is metabolized, it may
increase or decrease the level of the HCV DAA. This
would lead to either decreased efcacy or possibly
increased toxicity. Therefore, it is important to assess
concomitant medications for potential DDIs before
prescribing a HCV regimen that contains a DDI.
A helpful tool is located at http://www.hepatitisdruginteractions.org.26 This Web site provides
charts regarding DDIs to inform the prescriber. It
is useful to access this tool before selecting a
HCV regimen.
The American Association for the Study of Liver
Disease/IDSA has published guidance that provides
treatment recommendations. These could be used as
a resource to make treatment decisions.8 Once a
treatment regimen has been selected, a baseline HCV
viral load, complete blood count, and complete
metabolic panel should be ordered. Patients should
be instructed on the medication dosages and
schedule. Instructions to take simeprevir, sofosbuvir,
and ribavirin with food to improve absorption should
be given to patients. Adherence to the medication in
order to maintain a steady drug level and prevent
resistance should be emphasized. The follow-up
laboratory schedule should include a complete blood
count, complete metabolic panel, and HCV RNA
quantitative viral load at treatment weeks 4, 8, 12,
and 24 if necessary.
All individuals who undergo treatment for HCV
should be assessed for an end-of-treatment (EOT)
response, dened as aviremia at the termination of
treatment. Viremia at the EOT signies nonresponse.
Individuals with nonresponse should be reevaluated
for treatment.8,27
Volume 11, Issue 1, January 2015

POST-TREATMENT FOLLOW-UP OF INDIVIDUALS WITH

HCV INFECTION
Individuals Who Achieve an End of Treatment
Response Should Be Tested for an SVR

All treated individuals who achieve an EOT response

should be monitored in the post-treatment phase for
a SVR, dened as aviremia after the withdrawal of
treatment. Monitoring should be with a quantitative
HCV RNA viral load at post-treatment weeks 12
and 24. Individuals who remain aviremic at posttreatment week 12 and 24 should be considered to
have had their virus eradicated. Aviremia at posttreatment week 12 and 24 is widely accepted as a
durable cure. Viremia recurring after an end of
treatment response is dened as relapse. Individuals
whose virus has relapsed should be reevaluated for
treatment options. Thereafter, ongoing periodic
monitoring may be performed at the clinicians
discretion.8,27
Individuals Who Have Been Treated Should Be
Monitored for Resolution of Any Treatment-related
Side Effects

Post-treatment monitoring to ensure the resolution

of treatment-related adverse effects such as hemolytic
anemia, neutropenia, thrombocytopenia, hypothyroidism, and symptoms such as rash, headache,
cough, muscle aches, depression, irritability, hair
loss, insomnia, and anorexia is warranted and
should be individualized for each patient. Posttreatment monitoring includes interim history taking,
physical examination, and diagnostic testing.
Treatment side effects should be monitored to resolution and may be referred to another provider for
evaluation and/or monitoring. Interferon-related
hypothyroidism may initially occur as late as 1-2 years
after the completion of treatment. Therefore,
thyroxin and thyroid-stimulating hormone levels
should be checked at 1 and 2 years post-treatment.
Ribavirin is pregnancy category X. On-treatment
contraceptive measures by individuals with childbearing or child-fathering potential who received
ribavirin should be continued for 6 months posttreatment. Counseling to avoid pregnancy, at least
two reliable forms of effective contraception, and
routine pregnancy testing should be provided as
appropriate.27,28
www.npjournal.org

HCV eradication lowers the risk of progression of

liver brosis and all-cause mortality. Nevertheless,
individuals who achieve successful eradication of
their HCV infection will remain at risk, albeit
theoretically lower, for sequelae of liver disease progression if their baseline brosis is sufciently
advanced or if they have liver disease cofactors.
These include metabolic syndrome, alcohol use,
uncontrolled coinfection with HIV or hepatitis B,
or risk for liver injury from drugs or dietary
supplements. In the absence of the ability to
quantify risk in these individuals, they should
continue to be considered at risk and managed
appropriately.29
Individuals Should Be Monitored for Post-treatment
Progression of Fibrosis and the Complications
Associated

Although cessation of the progression of brosis and

histologic improvement have been shown to be
among the benets of treating HCV infection, these
may not occur to an extent that would modify an
individuals risk of decompensation. In the interim,
clinicians should maintain an elevated level of
suspicion with regard to monitoring individuals for
the progression of brosis and the complications
associated with hepatic decompensation post-treatment. Published guidelines for the management of
cirrhosis and surveillance for complications should be
followed in the care of those with suspected
advanced brosis.
The risk for hepatocellular carcinoma in
HCV infection is known to increase with brosis
progression and age. The risk of hepatocellular
carcinoma in the post-treatment phase is not well
understood.
Screening for hepatocellular carcinoma is
indicated in individuals with HCV who have
METAVIR stage F3 brosis or stage F4 cirrhosis.
Cases of hepatocellular carcinoma have been
observed at earlier METAVIR stages of brosis.
Therefore, hepatocellular carcinoma screening
may be undertaken at the clinicians discretion in
the absence of proven stage 3 or 4 brosis. In the
absence of guidelines to the contrary, these guidelines
should also be applied to individuals who have
been treated.
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Specic tests used to screen for hepatocellular

carcinoma are controversial. Ultrasonography and
serum alpha fetoprotein level are most commonly
used. Because of the increased sonographic echogenicity that is characteristic of chronic liver disease,
scanning by magnetic resonance imaging or computed tomography will sometimes be indicated to
rule out liver masses and may be used at the clinicians
discretion.30
Individuals Should Be Counseled Regarding Their
Post-treatment Status and Risk of Reinfection

Successful treatment of HCV infection results in

aviremia, but antibodies to the hepatitis C virus are
typically retained for life. It is important for treated
individuals to understand the signicance of retained
antibodies: they do not, in the absence of serum
HCV RNA, signify active chronic hepatitis C virus
infection.
Although antibodies to HCV are typically
retained postviral eradication, they do not convey
immunity. All aviremic individuals with HCV antibodies should be considered susceptible to reinfection. Populations at higher risk include people who
inject drugs and men who have sex with men.4
It is important that individuals who have been
successfully treated and those who are found to
have spontaneously cleared be counseled on their
risk of reinfection despite the persistence of HCV
antibodies.27
IMPLICATIONS FOR THE PRIMARY CARE NP

With the birth cohort screening recommendation

from the Centers for Disease Control and Prevention
and the US Preventive Services Task Force, there
will be an increase in the number of patients diagnosed with HCV.29 This will provide an opportunity
for primary care NPs to further evaluate these
patients and consider the patient for treatment.
The anticipated interferon-free regimens with
combinations of DAAs will provide improved tolerability and efcacy with SVR rates > 90% in most
patients. SVR has proven to be enduring and nearly
always tantamount to cure.25 Therefore, every
patient with chronic HCV infection should be
considered for treatment once the new regimens
are available. Successful treatment of HCV will
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prevent or reduce the risk of complications of

HCV including decompensated liver disease,
hepatocellular carcinoma, diabetes, neuropsychiatric
symptoms, cryoglobulinemia, and lymphoma.
The primary care NP will play an important role
in screening and treating HCV patients in the
future.
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enough? A call to screen for hepatitis C virus in persons from countries of
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combination with ribavirin as initial treatment for chronic hepatitis C. N Engl J
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3. Poynard T, Marcellin P, Lee S, et al. Randomised trial of interferon alpha 2b
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15. Afdahl N, Zeuzem S, Kwo P, et al. Ledipasvir and sofosbuvir for untreated
HCV genotype 1 infection. N Engl J Med. 2014;370:1889-1898.
16. Afdahl N, Reddy R, Nelson D, et al. Ledipasvir and sofosbuvir for
previously treated HCV genotype 1 infection. N Engl J Med.
2014;370:1483-1493.
17. Lawitz E, Poordad F, Pang P, et al. Sofosbuvir and ledipasvir xed-dose
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England; April 9-13, 2014.

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24. Jacobson I, Ghalib R, Rodriguez-Torres M, et al. SVR results of a once

daily regimen of simeprevir (TMC435) plus sofosbuvir (GS-7977) with or
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www.npjournal.org

Mary C. Olson, DNP, ANP-BC, is a research nurse manager at the

Center for the Study of Hepatitis C and faculty at the Weill Cornell
Medical College in New York City and Ira M. Jacobson, MD, is faculty
at Weill Cornell Medical College in New York, NY. Ms. Olson can be
reached at maa9041@med.cornell.edu. Donald Gardenier, DNP,
FNP-BC, is assistant professor and clinical program director at the Icahn
School of Medicine at Mount Sinai in New York City. In compliance
with national ethical guidelines, the author reports no relationships with
business or industry that would pose a conict of interest.
1555-4155/14/$ see front matter
2015 Elsevier, Inc. All rights reserved.
http://dx.doi.org/10.1016/j.nurpra.2014.10.013

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